Blood glucose normalization upon transplantation of human embryonic pancreas into beta-cell-deficient SCID mice

Abstract

Aims/hypothesis. Transplanting human pancreatic islet beta cells could represent a radical new treatment of Type I (insulin-dependent) diabetes mellitus. However, beta cells available for grafting are scarce and finding new sources of such cells would be crucial for any cell therapy for diabetes. Undifferentiated precursor cells present in the human embryonic pancreas could represent such a source. Methods. We grafted human embryonic pancreases (6-9 weeks of development) that contain very few beta cells onto NOD/scid mice. Results. The human pancreatic tissue grew, increasing in weight 200 times within six months and endocrine cells differentiated, the number of human beta cells being increased by a factor 5000. Finally, the developed human endocrine tissue was mature enough to control the glycaemia of mice deficient in endogenous beta cells. Conclusion/interpretation. Human embryonic pancreas represent a source of immature cells that can proliferate and differentiate into mass beta cells after transplantation. Transplantation of human embryonic pancreas into NOD/scid mice is a useful model for understanding the development of the human pancreas during prenatal life.